Electrophysiological effects of alpha-adrenoceptor stimulation in perfused and superfused myocardium

Abstract

To investigate possible mechanisms for the differing electrophysiological actions of α-adrenoceptor stimulation in superfused myocardium and isolated, perfused hearts, we compared the cellular electrophysiological responses to methoxamine (10 −7, 10 −6 and 10 −5 m) in isolated, buffer-perfused guinea-pig hearts and superfused right ventricular tissue at 32°C and 37°C. During superfusion at 32°C with 10 −7 m methoxamine, action potential duration increased. Similar increases in action potential duration and refractory period were seen with 10 −6 m methoxamine while with 10 −5 m methoxamine action potential duration increased but refractory period was unchanged. At 37°C, no changes occurred with 10 −7 m and 10 −6 m methoxamine hbut with 10 −5 m, action potential duration increased. Perfusion of isolated hearts with 10 −7 m and 10 −6 m methoxamine had no effect on action potential duration and refractory period at 32°C, but with 10 −5 m methoxamine, refractory period increased. No changes occurred in the hearts at 37°C. Methoxamine had no effect on maximum upstroke velocity of the action potential, conduction time, QRS width and pacing threshold in the perfused hearts or the superfused ventricular strips. Methoxamine (10 −6 m) also reduced action potential duration and refractory period in hearts made globally ischaemic, confirming previous results. Thus, methoxamine increases action potential duration and refractory period in superfused ventricular tissue (32°C > 37°C), has no effect in normally perfused hearts, but during myocardial ischaemia reduces action potential duration and refractory period.